Gout or deposition of monosodium urate crystalsDefinition, epidemiology and pathophysiology

The most common depositional arthropathy resulting from the deposition of monosodium urate crystals in and around the joints. It has a prevalence of between 0.1% and 10% in the world population and is more common in older men [2].

Primary or secondary hyperuricaemia predisposes to the formation of monosodium urate crystals around the joints, in the synovial fluid, enthesis or bone, leading to a local inflammatory response, synovitis and the formation of gouty tophi [14]. Gouty tophi are accumulations of crystals, proteins and lipids, surrounded by a granulomatous foreign body reaction, located in the hypodermis, joint or parapatellar space and tendons, most commonly the Achilles tendon, extensor mechanism and popliteus tendon [13, 20, 28]. However, there is a predilection for the first metatarsophalangeal joint of the foot with approximately 90% monoarticular presentation [14, 24].

Clinical presentation and general diagnostic approach

In clinical practice, it presents in four phases: asymptomatic, acute, intercritical and chronic. Acute crises are manifested by local inflammation and increased joint volume associated with systemic symptoms [21]. In the chronic phase, joints are bulky with nodules that may ulcerate and excrete whitish particulate material [24].

The GOLD standard for diagnosis is polarising microscopy, which identifies monosodium urate crystals after puncture of joint fluid or gouty tophi [21, 24]. However, the American College of Rheumatology and the European League Against Rheumatism have proposed diagnostic probability criteria using clinical, laboratory and imaging findings. A score > 8 provides specificity when imaging evaluation includes dual-energy US and CT scan for joint/bursa involvement or the presence of erosions on plain radiography [29].

Imaging approach

Plain radiography has low S and SP for detecting acute gouty crisis, which presents with joint effusion and unilamellar periosteal reaction due to adjacent inflammation [13, 14]. Chronic tophaceous gout typically presents with asymmetric polyarticular involvement of the lower limbs, often involving the Achilles tendon, olecranon bursa and extensor mechanism of the knee. Tophi appear as subcutaneous nodules of variable morphology, usually opaque and sometimes calcified [13, 14], with non-marginal or juxta-articular erosions with sclerotic contours, long and parallel to the long axis of the diaphysis [28] (Fig. 1).

Fig. 1

Radiograph of the right knee, anteroposterior (AP) and lateral (L) views, in a 52-year-old man with a 10-year history of chronic tophaceous gout presenting with purulent material oozing from a cutaneous nodule on the right knee. ABCDE’S radiographic approach: A: Adequate alignment. B: Enthesophytes of the extensor mechanism of the patella (red arrows), sclerosis and subchondral cysts (short white arrows) and decreased bone density. C: Symmetrically decreased joint space and increased amount of suprapatellar bursa fluid (blue bracket). D: Single joint. E: Long, parallel, sclerotic, non-marginal femorotibial and peroneal erosions (long white arrows). S: Thickening of the subcutaneous cellular tissue (yellow stars) and calcification projected on the suprapatellar bursa (green circle)

Ultrasound in acute gouty crisis shows the ‘double contour’ sign, a hyperechoic band of variable thickness on the articular cartilage, the ‘snowstorm’ sign with hyperechoic dots within an accumulation, and the ‘starry sky’ sign with articular effusion and internal hyperechoic foci less than 1 mm, together with findings of synovitis and bursitis [14, 20, 28] (Fig. 2). In chronic tophaceous gout, ultrasound shows tophi as well-demarcated, heterogeneous hypo-hyperechoic nodules with hyperechoic internal echoes, resembling ‘sugar lumps’ and possibly with posterior acoustic shadow [14, 20, 28]. Erosions are intra- or extra-articular with discontinuity of the cortex seen in two planes [14, 20, 28] (Fig. 2).

Fig. 2

B-mode ultrasound images using an 18 MHz linear transducer and AP x-ray magnification of the first metatarsophalangeal joint of the first toe of the left foot in a 45-year-old man with a history of chronic gout presenting with an acute crisis. The long soft arrow shows a non-marginal erosion of the metatarsal head, which on ultrasound shows joint effusion, synovial thickening and internal mobile particulate content forming the ‘starry sky’ sign compatible with urate crystal deposits. The yellow star shows oedema of the superficial periarticular soft tissues

Dual-energy computed tomography is indicated for diagnosis and follow-up, with S of 78–100% and SP of 89–100% [24]. It differentiates calcium from monosodium urate crystals using colour mapping [16], and the protocol includes the symptomatic joint, usually extending to the hands and feet if gout is suspected [16]. Although less useful in the early stages, it is the gold standard in chronic disease and characterises bone erosions and tophi seen at a density of around 160 HU [16]. However, it does not detect low density crystals or crystals less than 2 mm in diameter.

Magnetic resonance imaging evaluates only the symptomatic joint, including anatomical, fluid-sensitive and dynamically contrasted sequences [16]. In a gouty crisis, MR identifies bone marrow oedema, soft tissue oedema, joint effusion with internal particulate material, and synovitis (Fig. 3). In chronic gouty tophi, tophi appear as amorphous or nodular areas of low signal on T1, with variable signal on T2 (particularly isointense or hyperintense) and variable enhancement with contrast [16] (Fig. 3).

Fig. 3

Magnetic resonance images of the right knee, sagittal proton density, T2, T1 with contrast and SPAIR axial slices, of the patient described in Figure 1, where the long yellow arrows show low signal nodules without contrast enhancement located in the prepatellar soft tissues, and in particular one with contrast enhancement in the prefemoral region (long green arrow). The blue arrows show thickening and enhancement of the synovial membrane of the suprapatellar bursa with internal particulate effusion. Findings compatible with subcutaneous gouty tophi and findings due to acute synovitis

Calcium pyrophosphate deposition disease (CPPD)Definition, epidemiology and pathophysiology

Inflammatory arthropathy caused by the deposition of dehydrated calcium pyrophosphate crystals in and around the joints. It has three stages: chondrocalcinosis, pseudogout and pyrophosphate arthropathy, defined by the identification of calcium deposits by imaging/histology in hyaline or fibrous cartilage, clinical arthritic attacks and structural bone and cartilage changes due to calcium, respectively.

There is no gender predilection and the prevalence increases with age [2]. The pathophysiological mechanism is unknown, but it is thought that traumatic cartilage damage, ageing [2] or a metabolic disorder leads to excess pyrophosphate crystals, articular cartilage loss, local inflammation and synovitis [14, 30, 31].

Clinical presentation and general diagnostic approach

Mainly mono or oligoarticular presentation. EULAR (European League Against Rheumatism) describes 4 types of CPPD [30]; asymptomatic, which is the most common (10–20%) [14], associated with osteoarthritic changes, acute arthritis and chronic arthritis [30]. Definitive diagnosis requires identification of crystals by polarising microscopy. However, any patient over 65 years of age with clinical signs suggestive of inflammatory arthritis in non-weight-bearing joints other than the knee is highly suggestive of the disease.

Imaging approach

The imaging approach for chondrocalcinosis and pseudogout has been updated to align with the ACR (Rheumatology) and EAAR consensus CPPD 2023. Radiography remains the first-line modality, identifying thin, continuous or discontinuous, linear or patchy calcifications in the medial cartilage, typically 1–2 mm from the cortex [13, 14, 17]. These calcifications are common in the menisci of the knee, the triangular fibrocartilage of the wrist, the labrum of the shoulder and hip, and the symphysis pubis, and often appear as cloudy opacities in the synovial membrane or para-articular soft tissues, including tendons, bursae and ligaments [13, 14, 17]. Radiographic features of pyrophosphate arthropathy include involvement of the wrist, metacarpophalangeal joint, talocalcaneal–navicular joint, or elbow, with severely reduced joint space with few marginal osteophytes, subchondral cystic degeneration (geodes) and sclerosis without erosions, and free intra-articular bony bodies in the synovial membrane [13, 14, 17] (Fig. 4).

Fig. 4

AP and L views of the right knee in a 60-year-old woman with left-sided gonalgia associated with increased joint volume and documented signs of chondrocalcinosus and pyrophosphate arthropathy. Radiographic ABCDE’S approach: A: Adequate alignment B: Marginal osteophytes of the outer contours of the femoral condyle and lateral tibial plateau (white arrows). C: Radio-opaque punctate foci of lesser density than the bony cortex, located 1-2 mm from the bony cortex, located in the topography of the medial and lateral meniscus (green circles). D: Decreased femorotibial joint space, predominantly left. E: No erosions are observed S: Radio opaque cottony foci compatible with calcification of the fascia lata tendon and gastrocnemius muscle (orange arrows)

Ultrasound shows irregular linear or punctate echogenic crystal deposits in the center of the cartilage, often without posterior acoustic shadowing, highly specific for pyrophosphate arthropathy and associated with loss of cartilage thickness and intra-articular bodies [17, 28, 34]. These findings extend to the synovium, capsule, ligaments and tendons with inflammatory changes, forming the ultrasound sign of pseudo double contour (Ps-DC), as the crystalline deposits are also seen superficial to the hyaline cartilage, but during dynamic manoeuvres they move in the opposite direction to the cartilage, a characteristic finding that can differentiate it from monosodium urate deposition disease. [17, 28, 34, 39] (Fig. 5).

Fig. 5

FiB-mode ultrasound images with 18 MHz linear transducer and AP radiographic magnification of the most superficial sector of the external compartment of the right knee of the previous patient, showing, with green arrows, a linear arc-shaped echogenic deposit with posterior acoustic shadow, located in the centre of the lateral meniscus of the knee, whose presentation in the radiographic magnification is compatible with the deposit of the pyrophosphate crystal, the most specific finding for the disease. The white arrows indicate the marginal osteophytes, particularly of the lateral tibial plateau, and the yellow circle indicates the synovial effusion and thickening. Findings compatible with ultrasound manifestations of chondrocalcinosis and pyrophosphate atropathy

Conventional tomography shows linear or punctate calcifications of lower density than the bone cortex in hyaline or fibrous cartilage, with similar features in the synovial membrane, capsule, tendons, ligaments or bursae, manifesting as cloudy or hazy opacities in acute crises [16, 17] (Fig. 6).

Fig. 6

Enlargements of single tomography images of the right knee, coronal and sagittal reconstructions in bone window, in a 70-year-old patient who suffered a blunt trauma, where the green arrows show linear and some punctate calcifications with a density lower than the adjacent bone cortex, located in the medial and lateral menisci, as well as in the articular cartilage of the femoral condyle, as signs of incidental chondrocalcinosis. As an additional finding, the patient had a depressed fracture of the lateral tibial plateau requiring intervention

Magnetic resonance imaging detects cartilage calcifications by their low signal in all sequences, although it is more difficult to identify deposits in ligaments [16, 17].

Basic calcium deposition disease—hydroxyapatite arthropathyDefinition, epidemiology and pathophysiology:

Deposition of basic calcium, hydroxyapatite, octacalcium, tricalcium and whitlockite, in periarticular tissues, mainly in tendons and bursae [14], or in intra-articular locations, most commonly in rotator cuff tendons, gluteal muscles and rectus femoris muscles [2, 4, 13]. It affects adults aged 30–60 years, with a predilection for women, with an approximate prevalence of 3–8% in asymptomatic individuals and up to 42% in subacromial pain [4].

The pathophysiology remains unknown. It is thought to occur due to degenerative causes, ischaemia, trauma, chondrocyte mediated formation or endochondral ossification [25].

Uhthoff and Sarkar described three phases in the hydroxyapatite disease process; the pre-calcifying state, the calcifying state with its subdivisions of formative, quiescent and resorptive, and the post-calcifying state.

During the calcifying-resorptive phase, minor trauma or overuse of the joint can cause existing calcium crystals to become detached and shed into the surrounding tissue, leading to local inflammation, cartilage destruction, synovitis and chondrocyte apoptosis. This process is known as periarthritis or acute calcific arthritis and Milwaukee shoulder [4, 6, 25].

Clinical presentation and general diagnostic approach

Basic calcium deposition disease may present as asymptomatic calcifying tendinitis or Milwaukee shoulder [2]. The disease is predominantly monoarticular [